The present invention relates to apparatuses and methods for stents, and, more particularly to stents that opens in a blood vessel in a manner that avoids damage to arterial walls and dramatically reduces restenosis.
Angioplasty is commonly used to treat blockages of the coronary arteries, or peripheral arteries such as limbs. The balloon inserted into the narrow artery smashes the plaque against the artery wall. In the angioplasty procedure there is no choice but to expand the balloon until it causes damage to the internal stratum of the artery. This is done in order to reduce artery elasticity, preventing its contraction to the original state after balloon extraction.
A stent is a tube-like structure used in conjunction with angioplasty to permanently hold open an artery. Although stent implantation does not necessarily cause damage to artery wall stratum, and artery elasticity can be maintained to prevent artery contraction, the stent itself narrows the artery wall substantially in comparison to a balloon alone. In addition, during implantation of the stent the artery wall stratum is damaged and ripped, not because of artery wall extension but because of shifting and scraping of artery wall by the wires (i.e. struts) of the stent. The stent wires (struts) that generate the stent, work as blades that peel and penetrate the artery wall.
The occurrences of these scraping/lacerations are necessarily in the direction of a length and periphery of the artery. When the stent opens, the stent's periphery is widened. While the stent widens its periphery, the length of the stent contracts. Significant efforts are being made to develop a stent having a geometric structure such that the length of the stout will not be affected while the stent expands in the artery. However, even a stent that did not contract would still cause scraping and penetration of wires against the walls of the artery due to peripheral expansion. It should be noted that the stent's expansion in the artery, is on account of artery length. In order to solve this problem, an attempt exists to develop a stent that whose degree of contraction correlates with the degree of contraction of the artery.
Unfortunately, analyses that have addressed this issue demonstrate that as a whole this correlation is not possible. Accumulation of “rough” plaque in artery wall damages the artery's capability to expand its periphery and contracts its length with unity in a predictable matter. Therefore, up to now it has not been possible to correlate between stent contractions to artery contractions.
The relation between artery wall damage and restenosis has been researched extensively. Two or three weeks after stent implantation, there can be a return of artery blockage. This creates thrombosis that can be treated mainly by anti coagulating drugs. The chronic phase occurs generally between three to six months post implantation. The mechanism that causes the blockage in the chronic phase is not known. What is known is that there is a connection between artery wall injury that occurs while stent implantation and tissue growth within that creates a neointima layer after several months. It is also known that the artery can react to the stent, perceive it as a foreign object that penetrates artery wall, and respond with an immune system response that causes tissue growth. This leads to further narrowing of the artery near the stent or inside the stent.
In recent years, in order to find a solution to the problem of restenosis after angioplasty, there has been an effort to implant a stent coated with a given medication that is released over time. One of these stents is “full degradable” and the medication is released while the stent degrades. Medications of these sorts are supposed to treat the problem of tissue growth between and upon the stent wall, which develops several weeks after implantation. These drug-eluting stents are being tested clinically.
This problem of thrombosis, which appears in the artery a short while after implantation, is treated to some extent by the use of increased dosage of anti coagulating medications. Anti coagulating drugs and slow-release drugs prevent tissue growth within the stent. Stents coated with such medications treat the symptoms of a tear in the artery stratum after it happens but do not prevent the injury itself.
Significantly, moreover, the stents coated with drugs are very expensive. Although these stents inhibit tissue growth and thus may reduce the risk of restenosis from scar tissue and cell proliferation, to use these stents requires satisfying certain conditions and doing so requires a unique and complex procedure. One condition that must be satisfied, for example, is creating a drug that will be released in full in the two weeks time post implantation until several months later. In addition, the drug coating the stent should be a thin layer to avoid shortening the artery's diameter post implantation. The drug should also be flexible and not disengage during stent extension. These conditions make the product very expensive.
There is a compelling need for an apparatus that reduces the problems of prior art stents, namely, reducing scraping and penetration of artery walls by the stent when the stent opens, and damage to the artery wall when the stent length contracts during peripheral expansion.